MYOCARDIAL MORPHOMETRIC CHANGES RELATED TO DECREASED CONTRACTILITY AFTER ENDOTOXIN

Decreased ventricular contractility during sepsis lasts much longer th an the half-lives of inflammatory mediators that have been suggested t o be myocardial depressant factors. Our hypothesis is that blood-borne factors may also cause myocardial structural changes, including damag e and death of myocytes, associated with decreased ventricular contrac tility. We tested this hypothesis in an isolated rabbit. heart perfuse d by a support rabbit. Support rabbits received 1 mg/kg endotoxin iv o ver 30 min (endotoxin group, n = 7) or vehicle (control group, n = 6). The slope of the end-systolic pressure-volume relationship, E(max), w as used to measure contractility of the isolated heart. Five hours aft er endotoxin infusion, E(max) decreased by 17 +/- 7% (P < 0.03) compar ed with 0 +/- 2% in the control group. Quantitative morphometric analy sis of isolated hearts from the endotoxin group demonstrated an increa sed volume fraction of myocardial capillaries occupied by leukocytes ( 15.7 +/- 3.5 vs. 3.0 +/- 0.7% in the control group, P < 0.05), structu rally abnormal myocytes (7.6 +/- 3.6 vs. 0.8 +/- 0.4%, P < 0.05), and interstitial edema (23.2 +/- 5.2 vs. 14.3 +/- 2.1%, P < 0.05). We conc lude that blood-borne factors cause myocardial structural changes that may contribute to decreased ventricular contractility and may explain the prolonged decrease in ventricular contractility during sepsis.